traction. The follow-up period ranged from 3 to 14 months(average, 7 months), and the final postoperative visualacuity ranged from 20/25 to 20/400. Among the diabeticeyes, 5 eyes showed improvement of visual acuity by two ormore lines, 4 eyes were unchanged, and 1 eye was reduced(Case 9). All of the eyes with branch retinal vein occlu-sion and vitreous hemorrhage had improved visual acuityby two or more lines. The retinal thickness decreased anda foveal depression appeared in the postoperative opticalcoherence tomographic images in all eyes.

Macular edema is a frequent cause of visual impairment inpatients with retinal vascular diseases such as diabetic reti-nopathy and branch retinal vein occlusion. Lewis et al2

reported that peeling off the thickened vitreous membraneimproved visual acuity in diabetic macular edema, however,there are few morphological reports of the vitreomaculartraction in the secondary conditions.3 More recently, opticalcoherence tomographic images examination has enabled usto detect the fine structure of vitreoretinal interface connec-tions in idiopathic macular traction syndrome.4 Kishi andassociates5 found a posterior precortical vitreous pocket infront of the macular area, and postulated that a tractionalforce is generated in the anterior and tangential directionwhen the premacular vitreous cortex that forms the posteriorwall of the pocket shrinks in patients with idiopathic macularholes. In this study, the optical coherence tomographicimages of the vitreoretinal interface suggested a tangentialdirection of tractional force in 11 of 13 eyes, and mainly inthe anterior direction in two eyes. The configuration of thefovea improved after vitrectomy in all eyes, however, thepostoperative visual acuity may depend on existing retinalfunctional changes and the duration of the pathologicalconditions. Generally, vitreomacular traction syndrome rep-resents the condition of the eyes without other retinaldiseases.1,4 From our results, similar vitreomacular tractionsare observed in eyes with retinal diseases, although thedirection of the tractional force is somewhat different. Thevitreomacular traction with retinal diseases was detected byoptical coherence tomographic images more clearly becausethe direction of the traction was mainly tangential.

REFERENCES

1. Smiddy WE, Green WR, Michels RG, de la Cruz Z. Ultra-structural studies of vitreomacular traction syndrome. Am JOphthalmol 1989;107:177–185.

2. Lewis H, Abrams GW, Blumenkranz MS, Campo RV. Vitrec-tomy for diabetic macular traction and edema associated withposterior hyaloidal traction. Ophthalmology 1992;99:753–759.

3. Sebag J, Balazs EA. Pathogenesis of cystoid macular edema: ananatomic consideration of vitreoretinal adhesions. Surv Oph-thalmol 1984;28(Suppl):493–498.

4. Munuera JM, Garcia-Layana A, Maldonado MJ, Aliseda D,Moreno-Montanes J. OCT in successful surgery of vitreo-macular traction syndrome. Arch Ophthalmol 1998;116:1388–1389.

5. Kishi S, Hagimura N, Shimizu K. The role of the premacularliquefied pocket and premacular vitreous cortex in idiopathic

macular hole development. Am J Ophthalmol 1996;122:622–628.

Fluorescein Angiographic Findings inOcular SiderosisSaad Shaikh, MD, andMark S. Blumenkranz, MD

PURPOSE: To report a case of siderosis from a retainedintraocular iron foreign body manifesting localized retinalcapillary nonperfusion documented by fluorescein angiog-raphy.METHODS: Case Report. In a 35-year-old man with de-creased vision in the left eye, studies included fundusphotography, fluorescein angiography, visual field testing,and electrophysiology. Surgical foreign body extraction andhistopathologic examination were performed.RESULTS: Preoperatively, in the left eye, humphrey visualfields and electrophysiology testing revealed marked de-pression. Fluorescein angiography demonstrated nasalcapillary nonperfusion with occlusion of the second- andthird-order arterioles extending along a gradient from theforeign body. Microscopic examination of the lens cap-sule confirmed the diagnosis of siderosis secondary to aretained iron foreign body.CONCLUSION: Extensive capillary nonperfusion may beassociated with a retained iron intraocular foreign body,as documented by fluorescein angiography. (Am JOphthalmol 2001;131:136–138. © 2001 by ElsevierScience Inc. All rights reserved.)

THE FLUORESCEIN ANGIOGRAPHIC CHARACTERISTICS OF

ocular siderosis have rarely been described in the litera-ture. This is probably because the most common etiologicprecipitant, a retained metallic foreign body, necessitatesexpedient removal. The clinical manifestations of ocularsiderosis result from a chronic degenerative process presum-ably induced by the oxidation of reduced forms of elementaliron that result in the liberation of toxic oxidants. Findingsinclude iris heterochromia, mydriasis, cataract, lens disloca-tion or subluxation, and secondary glaucoma. The retina isexquisitely sensitive to iron toxicity and retinal detachment;retinal arteriolar narrowing as well as retinal pigment epithe-lial atrophy have also been documented.1 Electrophysiologictesting remains a sensitive test for siderosis with the electro-retinogram A wave initially decreased followed by completeextinction in long-standing cases.2 We present a case of

Accepted for publication Jul 17, 2000.From the Department of Ophthalmology, Stanford University Medical

Center, Stanford, California.Inquiries to Saad Shaikh, MD, Department of Ophthalmology, Stan-

ford University Medical Center, Boswell A157, Stanford, CA 94305; fax:(413) 826-4630; e-mail: saads@earthlink.net

AMERICAN JOURNAL OF OPHTHALMOLOGY136 JANUARY 2001

intraocular siderosis manifesting localized capillary nonperfu-sion documented by fluorescein angiography.

● CASE REPORT: A 35-year-old otherwise healthy malemechanic reported experiencing a foreign body sensationin his left eye immediately after hammering on an auto-mobile. The patient was examined at the time of injury,and his visual acuity was 20/20 bilaterally. In both eyes, theanterior segment, crystalline lens, and funduscopic exam-ination were within normal limits. No ocular lacerations orpenetrating wounds were encountered on examination.

Over the next few months, the patient had increasingocular irritation in the left eye accompanied by a decreasein vision that was treated by topical corticosteroids.

Repeat examination by a vitreoretinal surgeon 6 monthsafter the original incident revealed the visual acuity in his lefteye to be 20/150. Examination of the anterior and posteriorsegments of the right eye was entirely normal. In the left eye,the anterior segment demonstrated a slight xanthochromicdiscoloration of the anterior chamber fluid accompanied byearly iris heterochromia. The cornea and crystalline lens wereunremarkable. Funduscopic examination revealed sclerosis

FIGURE 1. (Left) Fundus photograph of the left eye reveals the encapsulated intraocular foreign body with adjacent reactivepigmentary changes. (Right) Right eye (OD) with normal electroretinogram combined (a), scotopic (b), and photopic (c) responsesas well as a normal flicker response (d). Left eye (OS) reveals corresponding minimal to absent responses.

FIGURE 2. Fluorescein angiogram of the left eye reveals normal posterior pole (A) but marked nasal capillary nonperfusion withocclusion of the second- and third-order arterioles extending along a gradient from the foreign body located in the inferonasalquadrant (B).

BRIEF REPORTSVOL. 131, NO. 1 137

and sheathing of the nasal retinal vessels. In the inferonasalquadrant, a rust-colored, linear metallic object measuringapproximately 3.0 mm 3 0.5 mm was discovered lying on theretinal surface at the equator and surrounded by reactiveretinal pigment epithelium changes (Figure 1, top). Theperifoveal retina demonstrated minimal thickening and asubtle color change manifested by a reddish glow. Alsopresent were golden opacities in the vitreous cavity. Theoptic disk was not pale but slightly hyperemic when com-pared with the right eye.

A computed tomography (CT) scan of the orbit con-firmed the presence of a refractile object in the inferonasalquadrant of the left eye. Humphrey visual fields (Hum-phrey Instruments, Dublin, California) revealed markeddepression in all quadrants with decreased central thresh-olds. Electrophysiologic testing revealed normal findings inthe right eye, but absent rod and cone responses in the lefteye. Additionally, only minimal flicker and combinedresponses were detected in the left eye (Figure 1, bottom).

In the left eye, fluorescein angiography of the posteriorpole demonstrated normal findings with brisk capillaryfilling (Figure 2, A). However, marked nasal capillarynonperfusion with occlusion of the second- and third-orderarterioles was observed extending along a gradient fromthe foreign body (Figure 2, B). Retinal pigment epitheliumatrophy and scarring resulted in staining adjacent to theretained foreign body. Given the clinical and diagnosticfindings, the presumptive diagnosis of siderosis secondaryto a retained intraocular iron foreign body was made.

The patient subsequently underwent a pars plana vit-rectomy to remove the foreign body. Intraoperative exam-ination revealed brown discoloration of the vitreous geland of portions of the lens capsule. An encapsulatedmetallic intraocular foreign body appeared to be wedged inthe retina in the inferonasal quadrant. Additionally, somesheathing of the peripheral retinal vessels and pigmentarydegeneration was observed, particularly in the inferonasalquadrant, but also extending into areas distant from theimpact site. Attempts to remove the object by an intraoc-ular magnet failed, and the capsule was then dissected free.It was found that the foreign body was anchored to thechoroid by a fibrous pedicle. Because of poor visualization,a lensectomy was performed, and after scissors were used tocut the fibrous pedicle, the foreign body was removedthrough the superonasal sclerotomy site.

Histopathologic examination of the lens capsule revealedperiodic acid Schiff (PAS)-positive tissue lined with epithe-lial cells containing brown cytoplasmic pigment granules.Iron staining was markedly positive. The intraocular foreignbody measured 5.0 3 1.0 3 1.0 mm on examination, wassliver shaped, and magnetic. Follow-up examination 3months postoperatively revealed a visual acuity of 20/60 inthe left eye but minimal improvement in funduscopic find-ings.

A computer Medline literature search revealed only 1previous report documenting the fluorescein angiographic

findings in ocular siderosis. Retinal pigment epitheliumdefects and cystoid macular edema were reported in a caseof a retained intraocular metallic stone.3 Iron deposits havea particular affinity for intraocular epithelial structures,such as lens and iris epithelium, but they have also beendemonstrated in the external limiting membrane of theretina and in the acid mucopolysaccharides of the perivas-cular tissue.4,5 Potent oxidants presumably liberated byelemental oxidation reactions result in degeneration of theinternal and external nuclear layers of the retina, prolifer-ation of the pigment epithelium, and subsequent narrow-ing of the retinal vasculature simulating a picture ofretinitis pigmentosa.3 In this case, a gradient response ofischemia was observed ranging from almost completevascular occlusion immediately adjacent to the intraocularmetallic foreign body to occlusion of the first- and second-order arterioles of the vasculature exiting the optic nervehead in the nasal hemisphere. This ischemic gradientlikely corresponded to a toxic diffusion gradient from theiron foreign body. Hence, this case documents the rarefluorescein angiographic findings associated with intraoc-ular siderosis but especially captures the progressive vascu-lar changes in a retinal ischemic and degenerative process.Additionally, it highlights the need for prompt diagnosisand management of retained intraocular foreign bodies.

REFERENCES

1. Sneed SR. Ocular siderosis. Arch Ophthalmol 1988;106:997.2. Schechner R, Miller B, Merksamer E, Perlman I. A long term

follow up of ocular siderosis: quantitative assessment of theelectroretinogram. Doc Ophthalmol 1990–1991;76:231–240.

3. Schocket SS, Lakhanpal V, Varma SD. Siderosis from aretained intraocular stone. Retina 1981;1:201–207.

4. Cibis PA, Brown EB, Hong SM. Ocular effects of systemicsiderosis. Am J Ophthalmol 1957;44:158–172.

5. Cibis PA, Yamashita T, Rodriguez F. Clinical aspects of ocularsiderosis and hemosiderosis. Arch Ophthalmol 1959;62:180–187.

Solitary Nonreactive ChoroidalTuberculoma in a Patient withAcquired Immune DeficiencySyndromeDavid A. DiLoreto, Jr., MD, PhD, andNarsing A. Rao, MD

Accepted for publication Jun 15, 2000.From the Department of Ophthalmology, University of Southern

California School of Medicine (D.A.D.), A. Ray Irvine Jr., MD, OcularPathology Laboratory, Doheny Eye Institute (D.A.D., N.A.R.). This workwas supported in part by NIH core grant EY03040, and by an unrestrictedgrant to the Doheny Eye Institute from Research to Prevent Blindness,New York, NY.

Inquiries to Narsing A. Rao, MD, Ocular Pathology Laboratory,Doheny Eye Institute, 1450 San Pablo Street, Los Angeles, CA 90033;Telephone: 323-442-6645; FAX: 323-442-6334.

AMERICAN JOURNAL OF OPHTHALMOLOGY138 JANUARY 2001